Neuroinflammation and Autophagy in Parkinson's Disease-Novel Perspectives.
Danail MinchevMaria KazakovaVictoria SarafianPublished in: International journal of molecular sciences (2022)
Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder. It is characterized by the accumulation of α-Synuclein aggregates and the degeneration of dopaminergic neurons in substantia nigra in the midbrain. Although the exact mechanisms of neuronal degeneration in PD remain largely elusive, various pathogenic factors, such as α-Synuclein cytotoxicity, mitochondrial dysfunction, oxidative stress, and pro-inflammatory factors, may significantly impair normal neuronal function and promote apoptosis. In this context, neuroinflammation and autophagy have emerged as crucial processes in PD that contribute to neuronal loss and disease development. They are regulated in a complex interconnected manner involving most of the known PD-associated genes. This review summarizes evidence of the implication of neuroinflammation and autophagy in PD and delineates the role of inflammatory factors and autophagy-related proteins in this complex condition. It also illustrates the particular significance of plasma and serum immune markers in PD and their potential to provide a personalized approach to diagnosis and treatment.
Keyphrases
- oxidative stress
- endoplasmic reticulum stress
- cell death
- cerebral ischemia
- signaling pathway
- traumatic brain injury
- lipopolysaccharide induced
- induced apoptosis
- dna damage
- diabetic rats
- ischemia reperfusion injury
- lps induced
- cognitive impairment
- gene expression
- genome wide
- spinal cord
- inflammatory response
- dna methylation
- molecular dynamics
- density functional theory